Class	Assessment
Class 1	Normal functional ability
Class 2	Ability to carry out normal activities, despite discomfort or limited mobility of one or more joints
Class 3	Ability to perform only a few of the tasks of the normal occupation or of self-care
Class 4	Complete or almost complete incapacity with the patient confined to wheelchair or to bed

such as osteomyelitis, osteomalacia, osteoporosis or tumours can cause limb pain. Inflammation of tendons (tenosynovitis) can produce local pain over the affected area.

Vascular disease may also produce pain in the limbs. Acute arterial occlusion causes severe pain of sudden onset, often with coolness or pallor. Chronic peripheral vascular disease can result in calf pain on exercise that is relieved by rest. This is called intermittent claudication. Venous thrombosis can also cause diffuse aching pain in the legs associated with swelling.

Spinal stenosis can cause pseudo-claudication—pain on walking but relieved by leaning forward.

Nerve entrapment and neuropathy can both cause limb pain which is often associated with paraesthesiae or weakness. The usual cause is synovial thickening or joint subluxation—especially for patients with rheumatoid arthritis. The vasculitis associated with the inflammatory arthropathies can also cause neuropathy leading to diffuse peripheral neuropathy or mononeuritis multiplex. Patients with chronic rheumatoid arthritis often develop subluxation of the cervical spine at the atlanto-axial joint. This is caused by erosion of the transverse ligament around the posterior aspect of the odontoid process (dens). The patient may describe shooting paraesthesiae down the arms and an occipital headache. Neck flexion leads to indentation of the cord by the dens and can cause tetraplegia or sudden death. The abnormality may be obvious on lateral X-rays of the cervical spine (Figure 9.3). Injury to peripheral nerves can result in vasomotor changes and severe limb pain. This is called causalgia. Even following amputation of a limb, phantom limb pain may develop and persist as a chronic problem.

Figure 9.3 Rheumatoid arthritis

Lateral X-ray of the cervical spine showing anterior subluxation of the anterior arch of the dens of the axis (C2, arrow).

Courtesy Canberra Hospital X-ray library.

Raynaud’s phenomenon

Raynaud’s phenomenon ^a is an abnormal response of the fingers and toes to cold. Classically, the fingers first turn white, then blue and finally red after exposure to cold. It is during the red phase that the pain may be most severe, but pain during the white stage may also be severe, as a result of ischaemia. Patients with Raynaud’s disease have Raynaud’s phenomenon without an obvious underlying cause. The disease tends to be familial and females are more likely to be affected. In connective tissue diseases, especially scleroderma, Raynaud’s phenomenon can occur and may lead to the formation of digital ulcers (Table 9.7).

TABLE 9.7 Causes of Raynaud’s phenomenon (white-blue-red fingers and toes in response to cold)

Reflex

Raynaud’s disease (idiopathic)

Vibrating machinery injury

Cervical spondylosis

Connective tissue disease

Scleroderma, diffuse or limited type

Mixed connective tissue disease

Systemic lupus erythematosus

Embolism or thrombosis

Buerger’s disease (thromboangiitis obliterans)—smokers

Haematological

Cold agglutinin disease

Poisons

Drugs: beta-blockers, ergotamine

Vinyl chloride

Dry eyes and dry mouth are characteristic of Sjögren’s syndrome (Table 9.8). This syndrome may occur in isolation (primary Sjögren’s) and is very common in association with rheumatoid arthritis and other connective tissue disease. Mucus-secreting glands become infiltrated with lymphocytes and plasma cells, which cause atrophy and fibrosis. The dry eyes can result in conjunctivitis, keratitis and corneal ulcers. Sjögren’s syndrome can also have an effect on other organs such as the lungs or kidneys.

TABLE 9.8 Clinical features of Sjögren’s syndrome

In this syndrome mucus-secreting glands are infiltrated by lymphocytes and plasma cells, which cause atrophy and fibrosis of glandular tissue.

1 Dry eyes: conjunctivitis, keratitis, corneal ulcers (rarely vascularisation of the cornea)

2 Dry mouth

3 Chest: infection secondary to reduced mucus secretion or interstitial pneumonitis

4 Kidneys: renal tubular acidosis or nephrogenic diabetes insipidus

5 Genital tract: atrophic vaginitis

6 Pseudolymphoma: lymphadenopathy and splenomegaly, which may rarely progress to a true (usually non-Hodgkin’s) lymphoma

Note: This syndrome occurs in rheumatoid arthritis and with the connective tissue diseases.

Red eyes

The seronegative spondyloarthropathies and Behçet’s ^b syndrome but not rheumatoid arthritis may be complicated by iritis (eye pain with central scleral injection—a ‘red eye’—radiating out from the pupil) (see Figure 9.51, page 279). In other diseases, such as Sjögren’s, red eyes may be due to dryness, episcleritis or scleritis.

Systemic symptoms

A number of other symptoms may occur with specific rheumatological diseases. Fatigue is common with connective tissue disease. Weight loss and diarrhoea may occur with scleroderma, because of small-bowel bacterial overgrowth. Mucosal ulcers are common in some connective tissue diseases such as systemic lupus erythematosus (SLE). Specific rashes can also occur. Generalised stiffness can be due to rheumatoid arthritis or scleroderma, but other causes include systemic infection (e.g. influenza), excessive exercise, polymyalgia rheumatica, neuromuscular disease (e.g. extrapyramidal disease, tetanus, myotonia, dermatomyositis) and hypothyroidism. Finally, on occasion fever may be associated with the connective tissue diseases, especially SLE, but infection should always be excluded.

Treatment history

Document current and previous anti-arthritic medications (e.g. aspirin, other non-steroidal anti-inflammatory drugs, gold, methotrexate, penicillamine, chloroquine, steroids, anti-tumour necrosis factor α therapy, or other biological agents). Any side-effects of these drugs (e.g. gastric ulceration or haemorrhage, from aspirin) also need to be identified. Ask about physiotherapy and joint or tendon surgery in the past.

Past history

It is important to inquire about any history of trauma or surgery in the past. Similarly, a history of recent infection, including hepatitis, streptococcal pharyngitis, rubella, dysentery, gonorrhoea and tuberculosis, may be relevant to the onset of arthralgia or arthritis. A history of tick bite may indicate that the patient has Lyme disease. Inflammatory bowel disease can be associated with arthritis, as described on page 191. A history of psoriasis may indicate that the arthritis is due to psoriatic arthropathy. It is also important to inquire about any history of arthritis in childhood. The smoking history is important: rheumatoid arthritis is more common in smokers, and smoking adds to their already increased risk of cardiovascular disease.

Social history

Determine the patient’s domestic set-up and occupation. This is particularly relevant if a chronic disabling arthritis has developed. Any history of sexually transmitted disease in the past is important, but non-specific urethritis and gonorrhoea are especially relevant.

Family history

Some diseases associated with chronic arthritis run in families. These include rheumatoid arthritis, gout and primary osteoarthritis, haemochromatosis, the seronegative spondyloarthropathies and inflammatory bowel disease. A family history of bleeding disorder may explain an acutely swollen tender joint in a boy (haemophilia).

Examination anatomy

Joint structures (Figure 9.4)

Inflammatory arthritis affects first the joint synovium. Thickening of this may be palpable and is called pannus. Later, destruction of surrounding structures including tendons, articular cartilages and the bone itself occur.

Figure 9.4 Hand bones and finger joint—a typical synovial joint

Joint pain may be well localised if there is inflammation close to the skin, but deeper joint abnormalities may cause pain to be referred. The areas where joint pain is felt correspond to the innervation of the muscle attached to that joint—the myotome. For example, the glenohumeral joint of the shoulder and the posterior scapular muscles are supplied from C5 and C6, so pain over the shoulder or scapula may arise from any structure supplied from these nerve roots—including the shoulder muscles and joints but also the C5 and C6 segments of the spine. Figure 9.1 shows a map of approximate referral patterns for important joints.

The extra-articular structures that surround a joint—the ligaments, tendons and nerves—may also be the source of joint pain. Disease of the joint itself tends to limit movement of the joint in all directions, both active movement (moved by the patient) and passive movement (moved by the examiner). Extra-articular disease causes variable limitation of movement in different directions, and tends to cause more limitation of active than of passive movement.

The rheumatological examination

There are certain established ways of examining the joints and related structures ³ and it is important to be aware of the numerous systemic complications of rheumatological diseases. The actual system of examination depends on the patient’s history and sometimes on the examiner noticing an abnormality on general inspection. Formal examination of all the joints is rarely part of the routine physical examination, but students should learn how to handle each joint properly and a formal examination is an important part of the evaluation of patients who present with joint symptoms or who have an established diagnosis and active symptoms. Diseases of the extra-articular soft tissues are particularly common.

General inspection

This is important for two reasons: first, it gives an indication of the patient’s functional disability, which is essential in all rheumatological assessments; and second, certain conditions can be diagnosed by careful inspection. Look at the patient as he or she walks into the room. Does walking appear to be painful and difficult? What posture is taken? Does the patient require assistance such as a stick or walking frame? Is there obvious deformity, and what joints does it involve? Note the pattern of joint involvement, which gives a clue about the likely underlying disease (Tables 9.2 to 9.4).

For a more detailed examination the patient should be undressed as far as practical, usually to the underclothes. Depending on the patient’s condition and the parts of the body to be examined, the examination may best be begun with the patient in bed, or sitting over the side of the bed or in a chair, or standing. The opportunity of watching the patient remove the clothes should not be lost because arthritis can interfere with this essential daily task.

Principles of joint examination

Certain general rules apply to the examination of all the joints and they can be summarised as: look, feel, move, measure, and compare with the opposite side.

Look

The first principle is always to compare right with left. Remember that joints are three-dimensional structures and need to be inspected from the front, the back and the sides. The skin is inspected for erythema indicating underlying inflammation and suggesting active, intense arthritis or infection, atrophy suggesting chronic underlying disease, scars indicating previous operations such as tendon repairs or joint replacements, and rashes. For example, psoriasis is associated with a rash and polyarthritis (inflammation of more than one joint). The psoriatic rash consists of scaling erythematous plaques on extensor surfaces. The nails are often also affected (page 252). Also look for a vasculitic skin rash (inflammation of the blood vessels of the skin), which can range in appearance from palpable purpura or livedo reticularis (bluish-purple streaks in a net-like pattern) to skin necrosis.

A small, firm, painless swelling over the back (dorsal surface) of the wrist is usually a synovial cyst—a ganglion.^c A larger, localised, soft area of swelling of the dorsum of the wrist generally indicates tenosynovitis.

Note any swelling over the joint. There are a number of possible causes: these include effusion into the joint space, hypertrophy and inflammation of the synovium (e.g. rheumatoid arthritis), or bony overgrowths at the joint margins (e.g. osteoarthritis). It may also occur when tissues around the joints become involved, as with the tendinitis or bursitis of rheumatoid arthritis. Swelling of the lower legs may be due to fluid retention, which is painless and can occur in association with inflammation anywhere in the leg. Painful swelling may result from inflammation of the ankle joints or tendons, or of the fascia, or from inflammatory oedema of the skin and subcutaneous tissue.

Deformity is the sign of a chronic, usually destructive, arthritis, and ranges from mild ulnar deviation of the metacarpophalangeal joints in early rheumatoid arthritis to the gross destruction and disorganisation of a denervated (Charcot’s ^d) joint (Figure 10.20, page 319). Deviation of the part of the body away from the midline is called valgus deformity, and towards the midline, varus deformity. For example, genu valgum means knock-kneed and genu varum, bow-legged.

Look for abnormal bone alignment. Subluxation is said to be present when displaced parts of the joint surfaces remain partly in contact. Dislocation is used to describe displacement where there is loss of contact between the joint surfaces.

Muscle wasting results from a combination of disuse of the joint, inflammation of the surrounding tissues and sometimes nerve entrapment. It tends to affect muscle groups adjacent to the diseased joint (e.g. quadriceps wasting with active arthritis of the knee) and is a sign of chronicity.

Feel

Palpate for skin warmth. This is done traditionally with the backs of the fingers where temperature appreciation is said to be better. A cool joint is unlikely to be involved in an acute inflammatory process. A swollen and warm joint may be affected by active synovitis (see below), infection (e.g. Staphylococcus) or crystal arthritis (e.g. gout).

Tenderness is a guide to the acuteness of the inflammation, but may be present over the muscles of patients with fibromyalgia. The patient must be told to let the examiner know if the examination is becoming uncomfortable. Tenderness can be graded as follows:

Grade I—patient complains of pain

Grade II—patient complains of pain and winces

Grade III—patient complains of pain, winces and withdraws the joint

Grade IV—patient does not allow palpation.

This may result from joint inflammation or from lesions outside the joints (periarticular tissues), including inflamed tendons, bursae, or attachments (entheses). Infected joints are extremely tender and patients will often not let the examiner move the joint at all. Palpation of a joint or area for tenderness must be performed gently, and the patient’s face rather than the joint itself should be watched for signs that the examination is uncomfortable.

Palpate the joint deliberately now, if possible, for evidence of synovitis, which is a soft and spongy (boggy) swelling. This must be distinguished from an effusion, which tends to affect large joints but can occur in any joint. Here the swelling is fluctuant and can be made to shift within the joint. Bony swelling feels hard and immobile, and suggests osteophyte formation or subchondral bone thickening.

Move

Much information about certain joints is gained by testing the range of passive movement. (Passive movement is obviously contraindicated in cases of recent injury to the limb or joint, such as a suspected fracture.) The patient is asked to relax and let the examiner move the joint. This must be attempted gently and will be limited if the joint is painful (secondary to muscle spasm), if a tense effusion is present, if there is capsular contraction or if there is a fixed deformity. The joints may have limited extension (called fixed flexion deformity) or limited flexion (fixed extension deformity). Passive movement of the spine is not a practical manoeuvre (unless the examiner is very strong), and active movement is tested here. Active movement is more helpful in assessing integrated joint function. Hand function and gait are usually applied as tests of function. Pain on motion indicates a joint or periarticular problem.

Stability of the joint is important and depends largely on the surrounding ligaments. This is tested by attempting to move the joint gently in abnormal directions to its usual limits, set by ligaments and muscular tone.

Joint crepitus, which is a grating sensation or noise from the joint, indicates irregularity of the articular surfaces. Its presence suggests chronicity.

Measure

Accurate measurement of the range of movement of a joint is possible with a goniometer, which is a hinged rod with a protractor in the centre. The jaws are opened and lined up with the joint. Measurement of joint movements is performed from the zero starting position. For most joints this is the anatomical position in extension—e.g. the straightened knee. Movement is then recorded as the number of degrees of flexion from this position. A knee with a fixed flexion deformity may be recorded as ‘30 to 60 degrees’, which indicates that there is 30 degrees of fixed flexion deformity and that flexion is limited to 60 degrees. At some joints both flexion and extension from the anatomical position can be measured, as at the wrists. The goniometer is not routinely used by non-rheumatologists and there is a wide range of normal values for joint movement. Most clinicians estimate the approximate joint angles.

A tape measure is useful for measuring and following serially the quadriceps muscle bulk and in examination of spinal movements.

Assessment of individual joints

The hands and wrists (Figures 9.5 to 9.9)

Examination anatomy

The articulations between the phalanges are synovial hinge joints. The eight bones of the wrist (carpal bones) form gliding joints which allow wrist movements—flexion/extension and abduction/adduction as they slide over each other.

Figure 9.5 Examination of the hands and wrists

Sitting up (hands on a pillow)

1. General inspection

Cushingoid

Weight

Iritis, scleritis, etc

Obvious other joint disease

5. Other

Elbows—subcutaneous nodules—psoriatic rash

Other joints

Signs of systemic disease

Figure 9.6 (right) X-ray of normal hand

Courtesy M Thomson, National Capital Diagnostic Imaging, Canberra.

Figure 9.7 Rheumatoid arthritis, early findings

X-ray of the hands of a patient with early rheumatoid arthritis. Note erosions of the heads of the metacarpophalangeal joints and of the ulnar styloid, and reduced amounts of cartilage in the joint spaces.

Courtesy Canberra Hospital X-ray library.

Figure 9.8 Rheumatoid arthritis, late findings

X-ray of the hands of a patient with advanced rheumatoid arthritis. Note loss of joint space and destruction of the right carpal joints, subluxation of metacarpophalangeal and poximal interphalangeal (PIP) joints, and Z deformity of the thumb. There are erosions of the PIP joints, a sign of active disease.

Courtesy Canberra Hospital X-ray library.

Figure 9.9 Osteoarthritis arthritis

X-ray of the hands showing the typical findings of osteoarthritis with joint-space narrowing and proliferative changes in the distal joints. Also note erosive and destructive changes at multiple proximal interphalangeal joints.

Courtesy Canberra Hospital X-ray library.

History

Pain may be present in some or all of the joints. It is more likely to be vague or diffuse if it has radiated from the shoulder or neck or is due to carpal tunnel syndrome, and to be localised if it is due to arthritis. Stiffness is typically worse in the mornings in rheumatoid arthritis. Swelling of the wrist may indicate arthritis or tendon sheath inflammation. Swelling of individual joints suggests arthritis. Deformity of the fingers and hand due to rheumatoid arthritis or of the fingers as a result of arthritis or gouty tophi may be the presenting complaint. The sudden onset of deformity suggests tendon rupture. Locking or snapping of a finger (trigger finger) is typical of inflammation of a flexor tendon sheath (tenovaginitis). Loss of function is a serious problem when it involves the numerous functions of the hand and wrist. The history should include an assessment of the difficulties the patient has in using the hands and wrists. Neurological symptoms as a result of nerve compression may cause paraesthesiae or limitation of strength or of complicated hand functions.

Examination

First sit the patient over the side of the bed and place the hands on the pillow with palms down. Often examination of the hands alone will give enough information for the examiner to make a diagnosis. As a result this is quite a popular test in viva voce examinations.

Look

Start the examination at the wrists and forearms. Inspect the skin for erythema, atrophy, scars and rashes. Look for swelling and its distribution. Next look at the wrist for swelling, deformity, ulnar and hyloid prominence. Then look for muscle wasting of the intrinsic muscles of the hand. This results in the appearance of hollow ridges between the metacarpal bones. It is especially obvious on the dorsum of the hand.

Go on to the metacarpophalangeal joints. Again note any skin abnormalities, swelling or deformity. Look especially for ulnar deviation and volar (palmar) subluxation of the fingers. Ulnar deviation is deviation of the phalanges at the metacarpophalangeal joints towards the medial (ulnar) side of the hand. It is usually associated with anterior (Volar) subluxation of the fingers (Figure 9.10). These deformities are characteristic but not pathognomonic of rheumatoid arthritis (Table 9.9).

Figure 9.10 The hands in rheumatoid arthritis

TABLE 9.9 Differential diagnosis of a deforming polyarthropathy

Rheumatoid arthritis

Seronegative spondyloarthropathy, particularly psoriatic arthritis, ankylosing spondylitis or Reiter’s disease

Chronic tophaceous gout (rarely symmetrical)

Primary generalised osteoarthritis

Erosive or inflammatory osteoarthritis

Now look for the characteristic changes of osteoarthritis (Figure 9.11). Here the distal interphalangeal and first carpometacarpal joints are usually involved. Heberden’s nodes^e are a common deformity caused by marginal osteophytes that lie at the base of the distal phalanx. Less commonly, the proximal interphalangeal joints may be involved and osteophytes here are called Bouchard’s^f nodes.

Figure 9.11 The hands (a) and the feet (b) of a patient with osteoarthritis

Showing Heberden’s nodes (distal interphalangeal joints), Bouchard’s nodes (proximal interphalangeal joints) and bunions.

Look also to see if the phalanges appear sausage-shaped. This is characteristic of psoriatic arthropathy, but can also occur in patients with Reiter’s disease. It is due to interphalangeal arthritis and flexor tendon sheath oedema. Finger shortening due to severe destructive arthritis also occurs in psoriatic disease and is called arthritis mutilans. The hand may take up a main en lorgnette (‘hand holding long-handled opera glasses’) appearance due to a combination of shortening and telescoping of the digits.

Now examine the nails. Characteristic psoriatic nail changes may be visible: these include pitting (small depressions in the nail), onycholysis (Figure 9.12) and, less commonly, hyperkeratosis (thickening of the nail), ridging and discoloration. The presence of vasculitic changes around the nailfolds implies active disease. These consist of black to brown 1–2 mm lesions due to skin infarction and occur typically in rheumatoid arthritis (Figure 9.13). Splinter haemorrhages may be present in patients with systemic lupus erythematosus (and infective endocarditis) and are due to vasculitis. Unlike nailfold infarcts they are located under the nails in the nail beds. Periungual telangiectasiae occur in systemic lupus erythematosus, scleroderma or dermatomyositis.

Figure 9.12 Psoriatic nails

Showing onycholysis and discoloration, with typical pitting and ridging.

Figure 9.13 Rheumatoid vasculitis (arrows)

The hands should now be turned over and the palmar surfaces revealed. Look at the palms for scars (from tendon repairs or transfers), palmar erythema, and muscle wasting of the thenar or hypothenar eminences (due to disuse, vasculitis or peripheral nerve entrapment). Telangiectasia here would support the diagnosis of scleroderma.

Feel and move

Turn the hands back again to the palm-down position. Palpate the wrists with both thumbs placed on the dorsal surface by the wrists, supported underneath by the index fingers (Figure 9.14). Feel gently for synovitis (boggy swelling) and effusions. The wrist should be gently dorsiflexed (normally possible to 75 degrees) and palmar flexed (also possible to 75 degrees) with the examiner’s thumbs. Then radial and ulnar deviation (20 degrees) is tested (Figure 9.15). Note any tenderness or limitation of movement or joint crepitus. Palpate the ulnar styloid for tenderness, which can occur in rheumatoid arthritis.

Figure 9.14 Palpating the wrist joint—approved method

Figure 9.15 Movements of the wrist

(a) Ulnar and radial deviation. (b) Dorsal and palmar flexion.

Test for tenderness at the tip of the radial styloid. This suggests de Quervain’s ^g tenosynovitis.

Feel for tenderness in the anatomical snuff box if scaphoid injury is suspected (Figure 9.15). Test for tenderness distal to the head of the ulna for extensor carpi ulnaris tendinitis.

Go on now to the metacarpophalangeal joints, which are palpated in a similar way with the two thumbs. Again passive movement is tested. Volar subluxation can be demonstrated by flexing the metacarpophalangeal joint with the proximal phalanx held between the thumb and forefinger. The metacarpophalangeal joint is then rocked backwards and forwards (Figure 9.16). Very little movement occurs with this manoeuvre at a normal joint. Considerable movement may be present when ligamentous laxity or subluxation is present.

Figure 9.16 Examination for volar subluxation at the metacarpophalangeal joints

Palpate the proximal and distal interphalangeal joints for tenderness, swelling and osteophytes.

Next test for palmar tendon crepitus. The palmar aspects of the examiner’s fingers are placed against the palm of the patient’s hand while he or she flexes and extends the metacarpophalangeal joints. Inflamed palmar tendons can be felt creaking in their thickened sheaths and nodules can be palpated. This indicates tenosynovitis.

A trigger finger may also be detected by this manoeuvre. Here the thickening of a section of digital flexor tendon is such that it tends to jam when passing through a narrowed part of its tendon sheath. Rheumatoid arthritis is an important cause. Typically, flexion of the finger occurs freely up to a certain point where it sticks and cannot be extended (as flexors are more powerful than extensors). The application of greater force overcomes the resistance with a snap.

If the carpal tunnel syndrome is suspected, ask the patient to flex both wrists for 30 seconds—paraesthesiae will often be precipitated in the affected hand if the syndrome is present (Phalen’s^h wrist flexion test). The paraesthesiae (pins and needles) are in the distribution of the median nerve (page 363), when thickening of the flexor retinaculum has entrapped the nerve in the carpal tunnel (Table 9.10). This test is more reliable than Tinel’s sign,ⁱ in which tapping over the flexor retinaculum (which lies at the proximal part of the palm) may cause similar paraesthesiae.⁴

TABLE 9.10 Causes of carpal tunnel syndrome

Carpal bone osteomyelitis

Now test active movements. First assess wrist flexion and extension as shown in Figure 9.17. Compare the two sides. Now go on to thumb movements (Figure 9.18). The patient holds the hand flat, palm upwards, and the examiner’s hand holds the patient’s fingers. Test extension by asking the patient to stretch the thumb outwards, abduction by asking for the thumb to be pointed straight upwards, adduction by asking him or her to squeeze the examiner’s finger, and opposition by getting the patient to touch the little finger with the thumb. Look for limitation of these movements and discomfort caused by them. Next test metacarpophalangeal and interphalangeal movements. As a screening test, ask the patient to make a fist then to straighten out the fingers (Figure 9.19). Then test the fingers individually. If active flexion of one or more fingers is reduced, test the superficial and profundus flexor tendons (Figure 9.20). Hold the proximal finger joint extended and instruct the patient to bend it; the distal fingertip will flex if the flexor profundus is intact. Then hold the other fingers extended (to inactivate the profundus) and check finger flexion (inability indicates the superficialis is unable to work). The most common tendon ruptures are of the extensors of the fourth and fifth fingers.

Figure 9.17 (a) Active wrist extension and (b) active wrist flexion

Figure 9.18 Thumb movements

(a) Extension. (b) Abduction. (c) Adduction. (d) Opposition.

Figure 9.19 Screening metacarpophalangeal and interphalangeal movements

(a) Flexion. (b) Extension.

Figure 9.20 Testing the superficial and profundus flexor tendons

(a) Flexor profundus. (b) Flexor superficialis.

Function

It is important to test the function of the hand. Grip strength is tested by getting the patient to squeeze two of the examiner’s fingers. Even an angry patient will rarely cause pain if given only two fingers. Serial measurements of grip strength can be made by asking the patient to squeeze a partly inflated sphygmomanometer cuff and noting the pressure reached. Key grip (Figure 9.21) is the grip with which a key is held between the pulps of the thumb and forefinger. Ask the patient to hold this grip tightly and try to open up his or her fingers. Opposition strength (Figure 9.22) is where the patient opposes the thumb and individual fingers. The difficulty with which these can be forced apart is assessed. Finally, a practical test, such as asking the patient to undo a button or write with a pen, should be performed.

Figure 9.21 The key grip

Figure 9.22 Testing opposition strength

Tests of hand function should be completed by formally assessing for neurological changes (page 362).

Examination of the hands is not complete without feeling for the subcutaneous nodules of rheumatoid arthritis near the elbows (Figure 9.23). These are 0.5–3 cm firm, shotty, non-tender lumps which occur typically over the olecranon. They may be attached to bone. They are found in rheumatoid-factor-positive rheumatoid arthritis. Rheumatoid nodules are areas of fibrinoid necrosis with a characteristic histological appearance and are probably initiated by a small vessel vasculitis. They are localised by trauma but can occur elsewhere, especially attached to tendons, over pressure areas in the hands or feet, in the lung, pleura, myocardium or vocal cords. The combination of arthritis and nodules suggests the diagnostic possibilities listed in Table 9.11.

Figure 9.23 Subcutaneous nodules in rheumatoid arthritis

TABLE 9.11 Causes of arthritis plus nodules ^*

Rheumatoid arthritis

Systemic lupus erythematosus (rare)

Rheumatic fever (Jaccoud’s^† arthritis) (very rare)

Granulomas—e.g. sarcoidosis (very rare)

^* Gouty tophi and xanthomata from hyperlipidaemia may cause confusion.

^† François Jaccoud (1830–1913), professor of medicine, Geneva.

Pain from the elbow is usually diffuse and may radiate down the forearm. It may occur over the lateral or medial epicondyle if the patient has tendinitis (tennis or golfer’s elbow). The patient may have noticed some swelling as a result of inflammation. Swelling over the back suggests olecranon bursitis. Stiffness may interfere with elbow movements and the patient may complain of difficulty combing the hair. When supination and pronation are affected the patient may complain of difficulty with carrying and holding. If the patient is aware of the elbow moving abnormally this suggests instability of the joint and may be a result of rheumatoid arthritis or trauma. Ulnar nerve trauma at the elbow may lead to a complaint of numbness or paraesthesiae in the distribution of that nerve.

Examination

Watch as the patient undresses, for difficulty disentangling the arms from clothing. The upper arms should be exposed completely. Note any deformity or difference in the normal 5–10 degree valgus position (carrying angle) as the patient stands with the palms facing forward.

Look for a joint effusion, which appears as a swelling on either side of the olecranon. Discrete swellings over the olecranon or over the proximal subcutaneous border of the ulna may be due to rheumatoid nodules, gouty tophi, an enlarged olecranon bursa or, rarely, to other types of nodules (Table 9.11).

Feel for tenderness, particularly over the lateral and medial epicondyles which may indicate tennis or golfer’s elbow, respectively. Palpate any discrete swellings. Rheumatoid nodules are quite hard, may be tender and are attached to underlying structures. Gouty tophi have a firm feeling and often appear yellow under the skin, but are sometimes difficult to distinguish from rheumatoid nodules. A fluid collection in the olecranon bursa is softly fluctuant and may be tender if inflammation is present. These collections are associated with rheumatoid arthritis and gout, but often occur independently of these diseases.

Small amounts of fluid or synovitis of the elbow joint may be detected by the examiner, facing the patient, placing the thumb of the opposite hand along the edge of the ulnar shaft just distal to the olecranon where the synovium is closest to the surface. Full extension of the elbow joint will cause a palpable bulge in this area if fluid is present.

Move the elbow joints passively. The elbow is a hinge joint. The zero position is when the arm is fully extended (0 degrees). Normal flexion is possible to 150 degrees. Limitation of extension is an early sign of synovitis.

If lateral epicondylitis is suspected, ask the patient to extend the wrist actively against resistance (see Figure 9.70, page 291). Test the range of active movements by standing in front of the patient and demonstrating. If there is any deformity or complaint of numbness, a neurological examination of the hand and arm are indicated for ulnar nerve entrapment.